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World J Gastroenterol. Mar 7, 2017; 23(9): 1521-1540
Published online Mar 7, 2017. doi: 10.3748/wjg.v23.i9.1521
Host pathogen interactions in Helicobacter pylori related gastric cancer
Magdalena Chmiela, Zuzanna Karwowska, Weronika Gonciarz, Bujana Allushi, Paweł Stączek
Magdalena Chmiela, Weronika Gonciarz, Bujana Allushi, Department of Immunology and Infectious Biology, Institute of Microbiology, Biotechnology and Immunology, Faculty of Biology and Environmental Protection, University of Lodz, Banacha, 90-237 Lodz, Poland
Zuzanna Karwowska, Paweł Stączek, Department of Genetics of Bacteria, Institute of Microbiology, Biotechnology and Immunology, Faculty of Biology and Environmental Protection, University of Lodz, Banacha, 90-237 Lodz, Poland
Author contributions: Chmiela M designed, wrote and supervised the manuscript; Karwowska Z, Gonciarz W and Allushi B designed and wrote a part of the manuscript, Stączek P pre-reviewed the manuscript.
Conflict-of-interest statement: No potential conflicts of interest.
Open-Access: This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
Correspondence to: Magdalena Chmiela, PhD, Professor, Department of Immunology and Infectious Biology, Institute of Microbiology, Biotechnology and Immunology, Faculty of Biology and Environmental Protection, University of Lodz, Banacha 12/16, 90-237 Lodz, Poland. chmiela@biol.uni.lodz.pl
Telephone: +48-42-6354186 Fax: +48-42-6655818
Received: August 24, 2016
Peer-review started: August 25, 2016
First decision: September 12, 2016
Revised: October 26, 2016
Accepted: February 16, 2017
Article in press: February 17, 2017
Published online: March 7, 2017
Abstract

Helicobacter pylori (H. pylori), discovered in 1982, is a microaerophilic, spiral-shaped gram-negative bacterium that is able to colonize the human stomach. Nearly half of the world's population is infected by this pathogen. Its ability to induce gastritis, peptic ulcers, gastric cancer and mucosa-associated lymphoid tissue lymphoma has been confirmed. The susceptibility of an individual to these clinical outcomes is multifactorial and depends on H. pylori virulence, environmental factors, the genetic susceptibility of the host and the reactivity of the host immune system. Despite the host immune response, H. pylori infection can be difficult to eradicate. H. pylori is categorized as a group I carcinogen since this bacterium is responsible for the highest rate of cancer-related deaths worldwide. Early detection of cancer can be lifesaving. The 5-year survival rate for gastric cancer patients diagnosed in the early stages is nearly 90%. Gastric cancer is asymptomatic in the early stages but always progresses over time and begins to cause symptoms when untreated. In 97% of stomach cancer cases, cancer cells metastasize to other organs. H. pylori infection is responsible for nearly 60% of the intestinal-type gastric cancer cases but also influences the development of diffuse gastric cancer. The host genetic susceptibility depends on polymorphisms of genes involved in H. pylori-related inflammation and the cytokine response of gastric epithelial and immune cells. H. pylori strains differ in their ability to induce a deleterious inflammatory response. H. pylori-driven cytokines accelerate the inflammatory response and promote malignancy. Chronic H. pylori infection induces genetic instability in gastric epithelial cells and affects the DNA damage repair systems. Therefore, H. pylori infection should always be considered a pro-cancerous factor.

Keywords: Helicobacter pylori, Host susceptibility, Carcinogenesis, Bacterial diversity

Core tip: In 1994 Helicobacter pylori (H. pylori) was classified by the International Agency for Research of Cancer as a class I human carcinogen for gastric cancer. Nearly 60% of the intestinal type gastric cancers are associated with H. pylori infections. Cancer risk rises if strain possess virulence factors: CagA, VacA and BabA. These bacteria promotes gastric carcinogenesis by increased DNA damage, impairment of repair processes, induction of mitochondrial DNA and genomic mutations. Nearly 98% of mucosa associated lymphoid tissue lymphomas are H. pylori dependent. We discuss correlation between H. pylori and gastric cancer in the light of bacterial and host genetic variability.